Three patterns of radiation injury after CNS RT:
- Acute: headache, sleepiness, worse neurologic deficits during or immediately after RT. Rarely seen with current protocols. Can be both prevented and treated with glucocorticoids.
- Early delayed: somnolence (children), Lhermitte's sign; within weeks to months of RT. Increased T2 signal and sometimes enhancement on MRI that can mimic tumor recurrence (pseudoprogression). Self-limited and improves with glucocorticoids; if very symptomatic may require resection.
- Late delayed: dementia or other progressive neurologic deficits; typically months to years after RT. White matter abnormalities on MRI (leukoencephalopathy) or ring-enhancing mass (radiation necrosis). PET can distinguish delayed necrosis from tumor recurrence as can MR perfusion sequences. Progressive radiation necrosis is best treated palliatively with surgical resection unless it can be managed with glucocorticoids. Radiation injury of large arteries accelerates the development of atherosclerosis, increasing the risk of stroke years after RT. Endocrine dysfunction due to hypothalamus or pituitary gland injury can be due to delayed effects of RT. Development of a second neoplasm after RT also is a risk year after exposure.
For a more detailed discussion, see DeAngelis LM, Wen PY: Primary and Metastatic Tumors of the Nervous System, Chap. 118, p. 598, in HPIM-19. |